ライフサイエンスコーパス: phenylpyridinium

1 ypical" Oct substrates, including 1-methyl-4-phenylpyridinium.

2 reactive microgliosis elicited by 1-methyl-4-phenylpyridinium.

3 reactive microgliosis elicited by 1-methyl-4-phenylpyridinium.

4 dine while retaining transport of 1-methyl-4-phenylpyridinium.

5 ng 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium.

6 c uptake of the organic cation 3H-1-methyl-4-phenylpyridinium (3H-MPP+) was significantly enhanced (8

7 ubstrates [3H]-histamine and [3H]-N-methyl-4-phenylpyridinium ([3H]-MPP+).

8 sitively charged phenyl radicals 3-dehydro-N-phenylpyridinium (a), N-(3-dehydro-5-chlorophenyl)pyridi

9 we use a fluorescent analogue of 1-methyl-4-phenylpyridinium, a neurotoxic metabolite and known subs

10 ransports organic cations such as 1-methyl-4-phenylpyridinium and cimetidine.

11 Furthermore, a group of phenylpyridinium and quinolinium compounds were used to

12 re conducted using [(3)H] MMP(+) (1-methyl-4-phenylpyridinium) as the marker ligand and various displ

13 cations, including the neurotoxin 1-methyl-4-phenylpyridinium, as substrates.

14 have found that 3,5-diacyl-1,2,4-trialkyl-6-phenylpyridinium derivatives constitute a novel class of

15 TAT-C24Scr, decreased AMPH-evoked 1-methyl-4-phenylpyridinium efflux.

16 lease of the toxic organic cation 1-methyl-4-phenylpyridinium from astrocytes and protects against 1-

17 nduced release of preloaded N-methyl-4-[(3)H]phenylpyridinium from superfused hDAT cells.

18 gnificant neuroprotection against 1-methyl-4-phenylpyridinium, glutamate, and nitric oxide-induced ne

19 ns were comparably susceptible to 1-methyl-4-phenylpyridinium-, glutamate-, or camptothecin-induced c

20 The affinity for hOCT was higher for 4-phenylpyridiniums > 3-phenylpyridiniums > quinolinium, i

21 hOCT was higher for 4-phenylpyridiniums > 3-phenylpyridiniums > quinolinium, indicating that substra

22 d cations, tetraethylammonium and 1-methyl-4-phenylpyridinium, i.e. the pH value did not have an effe

23 polycytidylic acid)-, HIV-1 Tat-, 1-methyl-4-phenylpyridinium(+)-, IL-1beta-, and IL-12 p40(2)-induce

24 on confers protection by blocking 1-methyl-4-phenylpyridinium-induced CHOP up-regulation, ER Ca(2+) s

25 PC12 and MN9D cells vulnerable to 1-methyl-4-phenylpyridinium-induced cytotoxic cell death by a mecha

26 phenyl-1,2,3,6-tetrahydropyridine/1-methyl-4-phenylpyridinium-induced dopaminergic neurotoxicity both

27 st, significantly reduced LPS- or 1-methyl-4-phenylpyridinium-induced dopaminergic neurotoxicity with

28 hagy and protects neurons against 1-methyl-4-phenylpyridinium-induced oxidative stress in an in vitro

29 2)O(2) and the Parkinsonian toxin 1-methyl-4-phenylpyridinium-induced PKCdelta cleavage, kinase activ

30 e type B)-catalyzed production of 1-methyl-4-phenylpyridinium ion (MPP(+)) and is likely to involve a

31 ted with an exogenous neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP(+)) significantly decreased TR

32 he oxidation of MPTP to the toxic 1-methyl-4-phenylpyridinium ion (MPP(+)), which then targets the do

33 al pharmacokinetics or content of 1-methyl-4-phenylpyridinium ion (MPP+), the active metabolite of MP

34 hallenged with the DA neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP+).

35 I inhibitors such as rotenone and 1-methyl-4-phenylpyridinium ion, known as a metabolite of 1-methyl-

36 I inhibitor such as rotenone and 1-methyl-4-phenylpyridinium ion.

37 m) = 329 mum), and the neurotoxin 1-methyl-4-phenylpyridinium (K(m) = 33 mum).

38 1-Methyl-4-phenylpyridinium, lipopolysaccharide (LPS), and rotenone

39 the well-established LPS and the 1-methyl-4-phenylpyridinium-mediated models of Parkinson's disease,

40 ss, and neurotoxicity produced by 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopamine (6-OHDA)

41 to compare fluorescent analogs of 1-methyl-4-phenylpyridinium (MPP(+)) as reporters for the human ser

42 ed with the parkinsonian toxicant 1-methyl-4-phenylpyridinium (MPP(+)) as well as in the substantia n

43 mphetamine-triggered DAT-mediated 1-methyl-4-phenylpyridinium (MPP(+)) efflux.

44 ochondrial calcium in response to 1-methyl-4-phenylpyridinium (MPP(+)) in human neuroblastoma SH-SY5Y

45 and by dopaminergic neurotoxins, 1-methyl-4-phenylpyridinium (MPP(+)) in vitro and in vivo by 1-meth

46 1-Methyl-4-phenylpyridinium (MPP(+)) is a neurotoxin that causes Pa

47 1-Methyl-4-phenylpyridinium (MPP(+)) is selectively toxic to dopami

48 The neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) produces mitochondria-targeted

49 allenging dopaminergic cells with 1-methyl-4-phenylpyridinium (MPP(+)), a neurotoxin that inhibits co

50 lecular mechanisms of toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), an ultimate toxic metabolite

51 the Parkinsonism-inducing toxin, 1-methyl-4-phenylpyridinium (MPP(+)), into dopaminergic terminals i

52 T), and a charged VMAT, substrate 1-methyl-4-phenylpyridinium (MPP(+)), reduced striatal CYAM.

53 ,2,3,6-tetrahydropyridine (MPTP), N-methyl-4-phenylpyridinium (MPP(+)), selectively destroys the dopa

54 ion and transport activity toward 1-methyl-4-phenylpyridinium (MPP(+)), serotonin (5-HT), and dopamin

55 1-Methyl-4-phenylpyridinium (MPP(+)), the active metabolite of the

56 1-Methyl-4-phenylpyridinium (MPP(+)), the toxic metabolite of 1-met

57 cumulation of radiolabeled DA and 1-methyl-4-phenylpyridinium (MPP(+)), was found to directly correla

58 g models of serum deprivation and 1-methyl-4-phenylpyridinium (MPP(+)), we investigated the mechanism

59 rons treated with the neurotoxin, 1-methyl-4-phenylpyridinium (MPP(+)), which induces conversion of e

60 ilar relative effects in blocking 1-methyl-4-phenylpyridinium (MPP(+))-mediated death of dopaminergic

61 te that minocycline inhibits both 1-methyl-4-phenylpyridinium (MPP(+))-mediated iNOS expression and N

62 nes using the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP(+)).

63 The compound 1-methyl-4-phenylpyridinium (MPP) is a selective inhibitor of mitoc

64 rototypic cationic substrates, 3) 1-methyl-4-phenylpyridinium (MPP), and 4) the novel fluorescent pro

65 Using 1-methyl-4-phenylpyridinium (MPP+) -treated C57 mice primary mesenc

66 exposure to the neurotoxic agents 1-methyl-4-phenylpyridinium (MPP+) and N-methyl-D-aspartate (NMDA).

67 ates the uptake of the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and the neurotransmitter dopamin

68 ns 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+) in a dopaminergic cell line.

69 ahydropyridine and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induce PD symptoms and recapitul

70 ctor (bFGF) could protect against 1-methyl-4-phenylpyridinium (MPP+) induced striatal damage in neona

71 1-Methyl-4-phenylpyridinium (MPP+) levels after MPTP administration

72 3) significantly greater striatal 1-methyl-4-phenylpyridinium (MPP+) levels, as compared to mice dose

73 e involvement of free radicals in N-methyl-4-phenylpyridinium (MPP+) toxicity is less clear.

74 erexpression inhibited endogenous 1-methyl-4-phenylpyridinium (MPP+) uptake activity in HeLa cells.

75 with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+), and GM1 ganglioside added after

76 ,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridinium (MPP+), exerts its lethal effect by inh

77 r to the dopaminergic neurotoxin, 1-methyl-4-phenylpyridinium (MPP+), has been shown to produce PD-li

78 rain neurons treated with 6-OHDA, 1-methyl-4-phenylpyridinium (MPP+), or alpha-synuclein fibrils (alp

79 uced Parkinson's disease involves 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of 1-meth

80 ts by altering striatal levels of 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of MPTP.

81 1-Methyl-4-phenylpyridinium (MPP+), the cytotoxic metabolite of 1-m

82 ith chemical structure similar to 1-methyl-4-phenylpyridinium (MPP+), the MPTP metabolite responsible

83 dsRNA (poly IC)-, HIV-1 Tat-, and 1-methyl-4-phenylpyridinium (MPP+)-, but not IFN-gamma-, induced mi

84 ns 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+).

85 rotransmitters and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+).

86 eurons to the complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+).

87 1 behaved like PMAT, transporting 1-methyl-4-phenylpyridinium (MPP+, an organic cation) but not uridi

88 on to dopaminergic loss following 1-methyl-4-phenylpyridinium/MPTP treatment, in vitro and in vivo.

89 with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium, N27 cells (dopaminergic neuron cell li

90 omplex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP(+)) on striatal and cortical neu

91 The neurotoxin MPP+ (1-methyl-4-phenylpyridinium), oxidative stress, or impairment of ce

92 N-methyl-4-phenylpyridinium, phenylethylamine, amphetamine, and met

93 he reaction of cytosine with the 3-dehydro-N-phenylpyridinium radical cation.

94 with tyramine and the neurotoxin 1-methyl-4-phenylpyridinium suggest that the flexibility of the sid

95 , and quinidine, but not by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium), decynium-22

96 im, and induces apoptosis only in 1-methyl-4-phenylpyridinium-treated cells.

97 This binding is lost following 1-methyl-4-phenylpyridinium treatment.

98 of monoamines and the neurotoxin 1-methyl-4-phenylpyridinium was significantly reduced in CP tissues

99 xposed to the mitochondrial toxin 1-methyl-4-phenylpyridinium were also partially protected by lactof

100 rkinson's disease-relevant toxin, 1-methyl-4-phenylpyridinium, whereas downregulation of orthodenticl